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Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib;Alpelisib treated bladder tumors

ABSTRACT: Nintedanib is a potent anti-fibrotic angio-kinase inhibitor, which has shown clinical efficacy in combination with chemotherapy in locally advanced muscle invasive BC patients. Nintedanib inhibits Fibroblast Growth Factor receptors (FGFRs), validated targets in patients with BC harboring FGFR3/2 genetic alterations. Here, we aimed at studying its mechanisms of action to understand therapy their combination (n=4). Reads were mapped separately against the human and mouse genomes to differentiate tumor vs. stromal expression changes

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE218575 | GEO | 2023/04/13

REPOSITORIES: GEO

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Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib;Alpelisib treated bladder tumors

Project description:Nintedanib is a potent anti-fibrotic angio-kinase inhibitor, which has shown clinical efficacy in combination with chemotherapy in locally advanced muscle invasive BC patients. Nintedanib inhibits Fibroblast Growth Factor receptors (FGFRs), validated targets in patients with BC harboring FGFR3/2 genetic alterations. Here, we aimed at studying its mechanisms of action to understand therapy their combination (n=4). Reads were mapped separately against the human and mouse genomes to differentiate tumor vs. stromal expression changes

2023-04-13 | GSE182833 | GEO

Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib Alpelisib treated bladder tumors

Project description:Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib Alpelisib treated bladder tumors

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Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib Alpelisib treated bladder tumors

Project description:Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib Alpelisib treated bladder tumors

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Nintedanib induces senolytic effect via STAT3 inhibition

Project description:Selective removal of senescent cells, or the concept of senolytic therapy, has been proposed to be a potent strategy for overcoming age-related diseases and even reversing aging. We found that nintedanib, a tyrosine kinase inhibitor, selectively induced cell death in primary human diploid fibroblasts undergoing replicative senescence. Similar to ABT263, a well-known senolytic agent, nintedanib triggered intrinsic apoptosis in senescent cells. Additionally, at the concentration producing the senolytic effect, nintedanib arrested the cell cycle of nonsenescent cells in the G1 phase without cytotoxicity. Interestingly, compared with ABT263, nintedanib showed a different mode of activating caspase-9 in the intrinsic apoptotic pathway, in that nintedanib did not suppress the levels of Bcl-2 family proteins in senescent cells. In more detail, nintedanib suppressed the activation of the JAK2/STAT3 pathway, which caused drug-induced cell death in senescent cells. STAT3 knockdown in senescent cells also induced caspase activation. Moreover, nintedanib reduced the number of senescent cells stained based on senescence-associated β-galactosidase activity and airway resistance in a mouse model of bleomycin-induced lung fibrosis. Overall, we identified that nintedanib could be used as a new senolytic agent and that inhibiting STAT3 could be a potential approach for inducing selective cell death in senescent cells. Our findings will pave the way for expanding senolytic toolkits in response to various aging statuses and age-related diseases.

2022-09-06 | GSE210020 | GEO

Gene Expression Changes Associated with Nintedanib Treatment in Idiopathic Pulmonary Fibrosis Fibroblasts [miRNA-seq]

Project description:We found strong protein-protein interactions within these dysregulated genes in nintedanib treated IPF fibroblast, with most genes involved in the pathways of cell cycle, mitotic cell cycle, and cell division. In IPF fibroblasts, we found nintedanib treatment was associated with downregulation of has-miR-92a-1-5p, which might de-repress SLC25A23 expression, and upregulation of has-miR-486-5p, which might repress DDX11, E2F1, and PLXNA4 expressions.

2019-04-08 | GSE124787 | GEO

Gene Expression Changes Associated with Nintedanib Treatment in Idiopathic Pulmonary Fibrosis Fibroblasts [RNA-seq]

2019-04-08 | GSE124786 | GEO

The Anti-Fibrotic Drug Nintedanib Promotes Expansion of Lung Macrophages with a Distinct Transcriptional Repair Program in Bleomycin-Exposed Mice

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressing chronic and fibrotic lung response with poor prognosis. The current standard-of-care for IPF is the kinase inhibitor nintedanib, which has a broad target range. The mechanism of nintedanib’s action remains unclear as it inhibits diverse kinases expressed in lung epithelia, endothelia and putatively the immune populations distributed throughout the lung. Given the proposed role of multiple pulmonary macrophage populations in mediating both protective and pathogenic roles in lung fibrosis, we sought to identify repair-associated macrophage populations in mice influenced by nintedanib after bleomycin challenge for 7 and 14 days using single cell RNA sequencing. Bleomycin exposure triggered expansion of inflammatory MHCIIhigh macrophage populations, which was partially reversed after nintedanib treatment. Concurrently, nintedanib promoted the expansion of MHCIIlow macrophages, which were linked to attenuation of lung fibrosis. Concomitantly, nintedanib promoted an increased expression of mRNA for canonical macrophage repair markers in MHCIIlow macrophages. Finally, exposure of inflammatory macrophages to nintedanib in vitro resulted in attenuation of expression of transcripts for MCHII. In conclusion, a component of nintedanib’s protective mode of action in lung fibrosis relies on expanding distinct MHCIIlow macrophage populations and redirecting them toward a reparative phenotype. This study provides a rationale for further refinement of therapeutic kinase inhibition in fibrotic diseases.

2021-05-05 | GSE151374 | GEO

Expression data from breast cancer tumors treated with a single window of the antiangiogenic agent Sunitinib

Project description:We have witnessed the rise and fall of antiangiogenic therapy in breast cancer (BC). Nevertheless, clinical remissions were observed in patients and we were interested in studying the activity of antiangiogenic drugs in BC. Inefficacy of sunitinib was observed in mouse models of metastatic BC, where evidence of enhanced metastasis was reported, and lack of efficacy of sunitinib-docetaxel combination was recently reported in a phase III clinical trial. Our aim was to understand the mechanisms and predictors of response to sunitinib in BC in a cohort of patients with untreated locally advanced or operable BC treated with an upfront window of single agent sunitinib, followed by the combination of sunitinib and docetaxel. We have used microarray profiing to monitor the transcriptional changes associated with three distinct stages of treatment: at diagnosis and prior to any treatment (t1), after an upfront window of single agent sunitinib (t2) and after the combined treatment of sunitinib and docetaxel (t3). In addtion, this microarray data also allowed us to observe the transcriptional changes associated with primary resistance to angiogenic therapy in 4 of 12 patients likely mediated by an adaptive transcriptional response to hypoxia in these resistant tumors. In BC patients this is the first demonstration of primary resistance to antiangiogenic therapy.

2016-12-31 | GSE58837 | GEO

Nintedanib induces senolytic effect via STAT3 inhibition

Project description:Nintedanib induces senolytic effect via STAT3 inhibition

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FGFR3-shRNA induced transcriptional changes in RT112 bladder cancer cells

Project description:Aberrant activation of FGFR3 via overexpression or mutation is a frequent feature of bladder cancer; however, its molecular and cellular consequences and functional relevance to carcinogenesis are not well understood. In this study with a bladder carcinoma cell line expressing inducible FGFR3 shRNAs, we sought to identiy transcriptional targets of FGFR3 and investigate their contribution to bladder cancer development. Bladder cancer cell line RT112 was transduced with a doxycycline-inducible control EGFP shRNA or three independent FGFR3 shRNAs, designated FGFR3 shRNA 2-4, FGFR3 shRNA 4-1 and FGFR3 shRNA 6-16. These four cell lines were treated with or without doxycycline for 48 hr to deplete FGFR3 protein prior to the isolation of mRNA for microarray analysis. Genes that were differentially expressed after doxycycline induction in all three FGFR3-depleted cell lines but not in the control cell line were considered potential FGFR3-regulated genes. Each treatment group was run in triplcates, and there are 24 samples.

2012-11-07 | E-GEOD-41035 | biostudies-arrayexpress

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